COPD

Michele Ritter, M.D.

Argy Teaching Resident, Feb. 2007

Definition

A disease state characterized by the presence of airflow obstruction due to chronic bronchitis or emphysema; the airflow obstruction is generally progressive, may be accompanied by airflow hyperactivity, and may be viewed as partially reversible.

Includes emphysema and chronic bronchitis

Prevalence

COPD occurs in 4-6% of white males, and 1-3% of adult white females

The 4th most common cause of death in the United States

14.2 million people in U.S. have COPDHighest mortality rate is in white men,

and the lowest is in hispanic women.

Types of COPD

Emphysema Permanent and destructive enlargement of airspaces

distal to the terminal bronchioles without obvious fibrosis and with loss of normal architecture

Always involves clinically significant airflow limitation. “pink puffer”

Chronic Bronchitis Presence of a cough productive of sputum not attributable

to other causes on most days for at least 3 months over 2 consecutive years

May be present in the absence of airflow limitation. “blue bloater”

COPD

Pathogenesis of COPD

Increased number of activated polymorphonuclear cells and macrophages produce elastases (such as human leukocyte elastase), resulting in lung destruction.

Increased oxidative stress caused by free radicals in cigarette smoke, the oxidants released by phagocytes, and polymorphonuclear leukocytes all may lead to apoptosis or necrosis of exposed cells

Pathogenesis of COPD (cont.) Emphysema

3 morphologic patterns:

Centricacinar: focal destruction limited to the

respiratory bronchioles and the central portions of acinus

associated with cigarette smoking

most severe in the upper lobes Panacinar:

involves the entire alveolus distal to the terminal bronchiole

develops in patients with homozygous alpha1-antitrypsin (AAT) deficiency

most severe in the lower lung zones

Distal acinar: Also called paraseptal least common form involves distal airway

structures, alveolar ducts, and sacs

localized to fibrous septa or to the pleura and leads to formation of bullae (can result in pneumothorax)

Chronic Bronchitis Mucus gland enlargement Airway atrophy, focal

squamous metaplasia, ciliary abnormalities, variable amounts of airway smooth muscle hyperplasia, inflammation, and bronchial wall thickening

Respiratory bronchioles display a mononuclear inflammatory process, lumen occlusion by mucous plugging, goblet cell metaplasia, smooth muscle hyperplasia, and distortion due to fibrosis

Airway walls to deform and narrow the airway lumen

Risk Factors

SMOKING! 48 million smokers in the U.S. 3000 new people take up smoking daily Nearly all patients with symptomatic

COPD are current or former smokers 10-20% of smokers will develop

symptomatic COPD. In men who smoke one pack/day, the

drop in FEV1 per year was 9 mL more than in non-smokers

Occupational Exposures Dusts, gases, fumes

Alpha1-antitrypsin deficiency Alpha1-antitrypsin is an important

protease inhibitor that usually presents elastases from causing lung destruction

Symptoms

DyspneaCough (usually worse in morning,

sputum production)WheezingCyanosisRight heart failureWeight loss, anorexia

Physical Exam

RR, HR, O2 saturation

Gen: Barrel-chest, accessory muscle use

CV: Quiet heart soundsResp: Decreased breath sounds,

wheezing, rhonchi, crackles

Labs

CBC: Hgb/HctABG: pH, pCO2

Chemistry: HCO3

Emphysema

Diagnosis of COPD

Look for secondary polycythemia: Hct >52% in males, Hct>47% in females

Measure alpha1-antitrypsin levels in all patients 40 years or younger, or in those with family history.

Hyperinflation see on chest x-rayBullae seen on Chest x-ray or CT scan

Pulmonary Function Tests

Diagnosis of COPD – Pulmonary Function Tests

Forced Expiratory Volume for 1 second (FEV1)

FEV1/FVC (Forced Vital Capacity) ratio Total Lung Capacity (TLC) Forced Residual Capacity (FRC) Residual Volume (RV) Vital Capacity (VC)

Pulmonary Function Tests

COPD Exacerbation

Typically manifest as increased sputum production, more purulent sputum and worsening of dyspnea.

Although infectious etiologies account for most exacerbations, exposure to allergens, pollutants or inhaled irritants may also play a role.

Bacterial infection is a factor in 70 to 75 percent of exacerbations, with up to 60 percent caused by

Streptococcus pneumoniae Haemophilus influenzae Moraxella catarrhalis

Antibiotic therapy has a small but important effect on clinical recovery and outcome.

Respiratory fluoroquinolone (Levofloxacin, Moxifloxacin) Ceftriaxone + azithromycin

Short courses of systemic corticosteroids may provide important benefits in patients with exacerbations of COPD.

Oxygen therapy to keep saturation Between 90-93% Non-invasive ventilation such as BiPAP can be helpful in avoiding

intubation/mechanical ventilation.

Treatment of COPD

SMOKING CESSATION! Short-acting bronchodilators

albuterol Long-acting bronchodilator

salmeterol Combination of anti-cholinergic and -agonist bronchodilator

Ipratropium + albuterol (combivent) Tiotropium (spiriva)

Methylxanthines (Theophylline) Has anti-inflammatory affect, and improves respiratory muscle function, stimulates

the respiratory center, and promotes bronchodilation Adverse effects include anxiety, tremors, insomnia, nausea, cardiac arrhythmia,

and seizures Inhaled corticosteroids

Fluticasone (Flovent), budesonide (Pulmicort) Combination of Inhaled corticosteroid and long-acting -agonist

Fluticasone + salmeterol (Advair) Oral Corticosteroids

Treatment of COPD (cont.)

Oxygen Therapy Continous oxygen has been shown to cut mortality in half or

decrease morbidity when compared with non-continous oxygen

Continuous (24 hours/day) Resting Pa02 of 55 mm HG, or Resting oxygen saturation < 88% Resting Pa02 of 56-59 mmHg or Oxygen Sat. <89% in presence of

dependent edema (suggestive of CHF), P pulmonale on ECG (P wave more than 3 mm in inferior leads) or cor pulmonale, or erythrocytosis (Hct > 56)

Noncontinuous During exercise – when PaO2 is < 55 mmHg or Oxygen sat. < 88%

with low level of exercise. During sleep if Pa02 is < 55 mmHg or Sa02 less than 88% with

associated complications such as pulmonary hypertension, daytime somnolence, cardiac arrythmias.

Treatment of COPD (cont.)

Pulmonary Rehabilitation Aimed at keeping patient conditioned with exercise,

perception of dyspnea, quality of life and self-efficacy.

Surgery Bullectomy

Resection of large bullae compressing normal lung

Lung volume reduction surgery Pneumonectomy of nonuniform emphysematous lung

Double lung transplantation Can be life-saving, but is costly, can be lack of donor

availability and requires lifelong immunosuppression.

Treatment of COPD

Stages of COPD

Stage FEV1/FVC Ratio

FEV1 %

Clinical Findings

At Risk >0.7 Patients who smoke, patients exposed to high pollutants, and patients with recurrent respiratory symptoms/infections. Give influenza and pneumonia vaccines.

Mild < 0.7 >80 Add short-acting bronchodilator as needed

Moderate <0.7 50-80 Add regular treatment with one or more long-acting bronchodilator and add Pulmonary rehabilitation

Severe <0.7 30-50 Add inhaled corticosteroids if repeated exacerbations

Very Severe

< 0.7 <30 Add long-term oxygen if chronic respiratory failure; Consider surgical treatments

Take Home Points

Smoking is the number one cause of COPD!

If smoking is stopped once COPD diagnosed, the progression of disease can slow down.

Treat COPD exacerbations with antibiotics and possibly with steroids.

Continuous oxygen is shown to decrease morbidity and mortality in COPD